A controlled trial of prostaglandin E1 precursor in chronic neuroleptic resistant schizophrenic patients

Vaddadi, Krishna S; Gilleard, Chris; Mindham, Richard; Butler, Richard J.

doi:10.1007/bf00180839

Cited by 53 publications

(9 citation statements)

References 15 publications

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“…There are reports of decreased levels of adrenic acid in medicated patients (Vaddadi et al, 1986; Yao et al, 1994) and in unmedicated patients (Peet et al, 2004). On the other hand, Richardson et al (2003) observed significantly elevated adrenic acid levels in adults with schizotypal personality traits.…”

Section: Discussionmentioning

confidence: 99%

Niacin sensitivity and the arachidonic acid pathway in schizophrenia

Messamore

Hoffman

Yao

2010

Schizophrenia Research

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Objective-Schizophrenia is associated with a blunted flush response to niacin. Since niacininduced skin flushing is mediated by vasodilators derived from arachidonic acid (AA), we tested whether the blunted flush response to niacin is a marker of AA deficiency.Methods-Eight concentrations of methylnicotinate were applied to the forearms of 20 adults with schizophrenia and 20 controls. Laser Doppler measurement of blood flow responses was used to derive values for niacin sensitivity (defined as the concentration eliciting half-maximal response, i.e., EC 50 value) and efficacy (defined as the maximal evoked blood flow response). RBC membrane fatty acids were analyzed by gas chromatography.Results-Niacin sensitivity and efficacy were reduced in schizophrenia. In the control group, there was significant correlation between AA levels and niacin sensitivity as well as a trend toward correlation between AA levels and niacin efficacy. In contrast, neither sensitivity nor efficacy of niacin correlated with AA levels in schizophrenia. An expected correlation between the levels of AA and its elongation product (adrenic acid) was absent in schizophrenia. Adrenic acid levels correlated with niacin efficacy in schizophrenia.Conclusions-The schizophrenia-associated niacin response abnormality involves both diminished sensitivity and reduced efficacy. The lack of expected correlation between levels of AA and adrenic acid suggests homeostatic imbalance within the n-6 polyunsaturated fatty acid (PUFA) pathway in schizophrenia. Though AA levels were unrelated to measures of niacin response in schizophrenia, the correlation between adrenic acid and niacin efficacy in schizophrenia suggests relevance of the n-6 PUFA pathway to the blunted niacin response.

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Section: Discussionmentioning

confidence: 99%

Niacin sensitivity and the arachidonic acid pathway in schizophrenia

Messamore

Hoffman

Yao

2010

Schizophrenia Research

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“…one capsule Efamol Evening Primrose Oil ® contains 360 mg LA, and 45 mg γ‐linolenic acid). Two initial small studies of Efamol Evening Primrose Oil ® supplementation in chronic patients with tardive dyskinesia (TD) did not identify any beneficial effect on TD or symptomatology [125,126]. However, in a double‐blind randomized, crossover study [127] there was marginal improvement in TD but an unexpected moderate improvement in psychopathology (20−30%) and overall cognitive functioning.…”

Section: Methodsmentioning

confidence: 99%

Implications of lipid biology for the pathogenesis of schizophrenia

Berger¹,

Wood

Pantelis

et al. 2002

Aust NZ J Psychiatry

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Peripheral blood cell, brain necropsy and 31P-MRS analysis reveal a disturbed lipid biology, suggesting generalized membrane alterations in schizophrenia. 31P-MRS data suggest increased membrane turnover at illness onset and persisting membrane abnormalities in established schizophrenia. Cellular processes regulating membrane lipid metabolism are potential new targets for antipsychotic drugs and might explain the mechanism of action of treatments such as eicosapentaenoic acid.

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“…Low AA levels have been identified in red blood cell (RBC) membranes from patients with chronic SZ (Glen et al, 1994;Peet et al, 1994;Vaddadi et al, 1986;Yao et al, 1994a), as well as first-episode neuroleptic-naïve SZ (Avrindakshan et al, 2003;Reddy et al, 2004). Thus, abnormally low AA levels have been observed in brain as well as RBC membrane phospholipids from patients with SZ (further reviewed by Conklin et al, 2007;Peet, 2007;Skosnik and Yao, 2003;Yao, 2003).…”

Section: Phospholipid Arachidonate and Eicosanoid (Pae) Signaling In Szmentioning

confidence: 99%

Phospholipid, arachidonate and eicosanoid signaling in schizophrenia

Messamore

Yao

2015

OCL

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-This paper reviews the potential role of arachidonic acid in the pathophysiology of schizophrenia. We discuss how abnormal levels of arachidonic acid may arise, and how dysregulation of signaling molecules derived from it have the potential to disrupt not only dopamine signaling, but numerous other physiological processes associated with the illness. Pharmacological doses of niacin stimulate the release of arachidonic acid; and arachidonic acid-derived molecules in turn dilate blood vessels in the skin. A blunted skin flush response to niacin is reliably observed among patients with schizophrenia. The niacin response abnormality may thus serve as a biomarker to identify a physiological subtype of schizophrenia associated with defective arachidonic acid-derived signaling.Keywords: Phospholipids / arachidonic acid / eicosanoids / niacin-induced flushing, endophenotype marker / schizophrenia Résumé -Signalisation des phospholipides, de l'arachidonate et de l'écosanoïde dans la schizophrénie. Cet article examine le rôle potentiel de l'acide arachidonique dans la physiopathologie de la schizophrénie. Il est discuté comment des niveaux anormaux d'acide arachidonique peuvent survenir, et comment la dérégulation des molécules de signalisation qui en découle est capable de perturber non seulement la signalisation de la dopamine, mais aussi de nombreux autres processus physiologiques associés avec cette maladie. Des doses pharmacologiques de niacine stimulent la libération d'acide arachidonique ; des molécules dérivées de l'acide arachidonique dilatent à leur tour les vaisseaux sanguins dans la peau. Une brusque rougeur de la peau en réponse à la niacine est observée de manière constante parmi les patients atteints de schizophrénie. La réponse anormale à la niacine peut donc servir de biomarqueur afin d'identifier un sous-type physiologique de la schizophrénie, associé à un système défectueux de signalisation des dérivés de l'acide arachidonique.

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A controlled trial of prostaglandin E1 precursor in chronic neuroleptic resistant schizophrenic patients

Cited by 53 publications

References 15 publications

Niacin sensitivity and the arachidonic acid pathway in schizophrenia

Niacin sensitivity and the arachidonic acid pathway in schizophrenia

Implications of lipid biology for the pathogenesis of schizophrenia

Phospholipid, arachidonate and eicosanoid signaling in schizophrenia

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